Abstract
Increasing evidence suggest that melatonin (N-acetyl-5-methoxytryptamine), an indolic compound identified from the pineal gland of mammals, regulates plant disease resistance. Here, we show that melatonin promoted susceptibility of salicylic acid (SA)-deficient Arabidopsis plants to the virulent bacterium Pseudomonas syringae, but enhanced resistance of jasmonic acid (JA)-insensitive mutants, ethylene (ET)-insensitive mutants, and abscisic acid (ABA)-biosynthetic mutants. However, melatonin had no effects on wild type Arabidopsis plants defending against P. syringae. In wild type Arabidopsis leaves, melatonin enabled to elevate endogenous SA and ABA levels and reduced JA and JA-isoleucine accumulation. In addition, melatonin induced the transcripts of SA-dependent pathogenesis-related protein 1 and JA/ET-dependent plant defensin 1.2. Furthermore, melatonin could affect neither pathogen-associated molecular pattern-triggered immunity nor avirulent effector-triggered immunity. Since ABA and JA/ET signaling antagonize SA-dependent disease resistance, our results thus clarify that defense-related hormone signaling, but not basal immune events, cooperatively determine the destiny of melatonin during Arabidopsis thaliana-P. syringae interaction.
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